As it is well established that cardiac abnormalities are lacking in these DMD/BMD mouse models, even in young adult animals (e.g., [40,98,99]), these Na+ channel defects in dystrophic neonatal cardiomyocytes can be considered primary effects of the dystrophin gene mutation, which precede cardiomyopathy development. This evidence concerns the gene DMD and Duchenne muscular dystrophy.